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Advances in immunology Volume 117/
Advances in Immunology, a long-established and highly respected publication, presents current developments as well as comprehensive reviews in immunology. Articles address the wide range of topics that comprise immunology, including molecular and cellular activation mechanisms, phylogeny and molecul...
| Clasificación: | Libro Electrónico |
|---|---|
| Otros Autores: | |
| Formato: | Electrónico eBook |
| Idioma: | Inglés |
| Publicado: |
Amsterdam ; Boston :
Elsevier/AP,
2013.
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| Edición: | 1st ed. |
| Colección: | Advances in immunology ;
v. 117. |
| Temas: | |
| Acceso en línea: | Texto completo Texto completo |
Tabla de Contenidos:
- Front Cover; Advances in Immunology; Copyright; Contents; Contributors; Chapter One: Mechanisms of Epigenetic Regulation of Leukemia Onset and Progression; 1. Introduction; 1.1. Leukemia as a heterogeneous and multifactorial disease; 1.1.1. Chronic myeloid leukemia; 1.1.2. Acute myeloid leukemia; 1.1.3. Acute lymphoblastic leukemia; 1.1.4. Chronic lymphocytic leukemia; 1.2. Epigenetic factors and their possible roles in leukemia; 2. Aberrant DNA Methylation in Leukemia; 2.1. The role of DNA methylation in hematopoietic malignancies; 2.2. The role of DNMT3A in leukemia
- 2.2.1. DNMT3A mutations in hematopoietic malignancies2.2.2. Functional consequence of DNMT3A mutations; 2.2.3. Mouse models of DNMT3 function; 2.2.4. Is mutant DNMT3A a prognostic marker in myeloid leukemia?; 2.2.5. DNMT inhibitors; 2.3. The biology of TET proteins and their perturbations in leukemia; 2.3.1. TET proteins; 2.3.2. Mutational status of TET proteins in leukemia; 2.3.3. Consequence of TET2 mutations in AML; 2.3.4. TET2 mouse models; 2.4. IDH1 and IDH2 oncometabolic proteins; 2.4.1. IDH1 and IDH2 mutations in leukemia; 2.4.2. Consequence of IDH mutations
- 2.4.3. Animal models for IDH gene function3. Disruption of Histone-Modifying Complexes Polycomb and MLL in Leukemia; 3.1. PRC2 in hematological neoplasms; 3.2. Role of PRC1 in leukemia; 3.2.1. Histone methyltransferase inhibitors; 3.3. MLL function; 3.3.1. MLL fusions in leukemia; 4. Other Epigenetic Writers, Erasers, and Readers; 4.1. Arginine methyltransferases; 4.2. Lysine demethylases (KDMs); 4.3. Histone demethylases inhibitors (KDMi); 4.4. Histone acetyl transferases; 4.4.1. HAT inhibitors; 4.5. Histone deacetylases; 4.5.1. HDAC inhibitors; 4.6. Bromodomain-containing proteins
- 4.6.1. BRD inhibitors4.7. Plant homeodomain-containing proteins; 4.8. Chromatin remodeling complexes; 5. Novel Aspects and Technologies in Epigenetics: Implications for Leukemia; 5.1. Combinatorial epigenetic marks; 5.2. Novel aspects of regulation and epigenetic factors in cancer; Acknowledgments; References; Chapter Two: Translocations in Normal B Cells and Cancers: Insights from New Technical Approaches; 1. Mechanistic Elements that Generate Chromosomal Translocations; 1.1. DNA DSB formation; 1.1.1. Physiologic breaks induced by RAG1/2 and AID enzymatic activity
- 1.1.1.1. RAG-initiated DSBs and translocations1.1.1.2. AID-initiated DSBs and translocations; 1.1.2. Pathologic induction of DSBs in normal and tumor cells; 1.2. DNA-repair mechanisms involved in translocations; 1.3. Chromosome territories and gene proximity in translocations; 1.4. Spatial organization of the genome: Implications for translocations; 2. Novel High-Throughput Methods to Study Chromosomal Translocations; 2.1. High-throughput genomic translocation sequencing; 2.2. Translocation-capture sequencing; 3. New Findings on Translocation Formation Obtained by HTGTS and TC-Seq